Forty years ago, if you were diagnosed as having lupus, otherwise known as systemic lupus erythematosus (SLE), the prognosis would not have been good. Odds were that you would have a 50/50 chance of dying within five years. Today doctors are most lik
Lupus is a baffling disorder with a multitude of symptoms and a different pathogenesis in each individual. Diagnosing this disorder, which affects nine times more women than men, can be difficult.
Although the general consensus is that it affects around 1 in 1000 people in Europe and America, recent research shows that it is underdiagnosed and that rates may be double what we have previously assumed (Lancet, 1996; 347: 367-9).
Lupus is an autoimmune disease which causes inflammation of the connective tissue, in particular of the membranes around the joints (with symptoms similar to those of rheumatoid arthritis) and around such organs as the lungs, kidneys and heart. Its most well known characteristic, however, is a red rash on the cheeks. In some cases this rash may spread to the entire upper body.
The less common form of lupus, discoid lupus erythematosus (DLE) presents as a red, scaly rash on the face the "wolf mask" from which lupus derives its name. DLE can remain static or it can turn into SLE the most common and severe form of lupus. When this happens the body begins to form antibodies against itself, causing inflammation, tissue damage and pain. Lupus can affect virtually any organ or system within the body and it can be life threatening.
The criteria for diagnosing lupus has not been revised since 1982 (Arthritis Rheum, 1982; 25: 1271-7), which may account for so many cases going undetected. When a physician is attempting to diagnose lupus, one of the first things he will check will be the patient's levels of anti nuclear antibodies (ANA). Some 95 per cent of lupus sufferers will have raised ANA (Rheum Dis Clin North Am, 1990; 16:617-39). ANA is common in other rheumatic diseases and in autoimmune liver and thyroid diseases. It is also present in around 2 per cent of the population without producing symptoms (Adv Immunol, 1989; 44: 93-151). There will also be a higher level of foreign DNA (Arthritis Rheum, 1990; 33: 634-43). In fact, SLE patients produce a large number of antibodies and, depending on which are present, physicians can predict with some certainty how the disease will develop (Clin Exp Immunol, 1985; 62: 337-45; J Clin Immunol, 1991; 11: 297-316).
What confounds doctors is what causes the immune system to go haywire in the first place. As with so many autoimmune disorders, doctors' bewilderment leads them to assume that SLE can't be cured and so they concern themselves more with what can be done to suppress and control symptoms. Because SLE patients can have a wide variety of symptoms, often it is treated in a rather haphazard way with courses, cocktails even, of drugs in the hopes that one of them will do the trick.
What this means is that, although more people are surviving SLE, they are at best living with a vastly decreased quality of life, and at worst, trading the risk of death from lupus for the risk of death from the drugs used to control it. For instance, one of the most common treatments is steroids, such as prednisone or prednisolone, to suppress the action of the immune system. These are given either as creams or in pill form. The side effects of steroids are wide ranging and too serious to use on a just in case basis. At one end of the spectrum they include weight gain, puffiness in your face and easy bruising. At the other extreme patients will suffer osteoporosis (Ann Int Med, Nov 15, 1993; Clin Pharm, 1993; 25(2): 126-35), muscle wastage (Euro Respir J, 1992; 5(8): 997-1003; Pol Tygo Lekar, 1989; 44(27): 6324), cataracts (Dermatol Clin, 1992; 10: 505-12; Surv Opthamol, 1986; 31: 2602) diabetes, hypertension and increased susceptibility to infection.